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Review
. 2021 Jan 28;10(3):479.
doi: 10.3390/jcm10030479.

Current Knowledge and Future Challenges in Takotsubo Syndrome: Part 1-Pathophysiology and Diagnosis

Elias Rawish  1   2 , Thomas Stiermaier  1   2 , Francesco Santoro  3 , Natale D Brunetti  3 , Ingo Eitel  1   2
Affiliations
Review

Current Knowledge and Future Challenges in Takotsubo Syndrome: Part 1-Pathophysiology and Diagnosis

Elias Rawish et al. J Clin Med. .

Abstract

First recognized in 1990, takotsubo syndrome (TTS) constitutes an acute cardiac condition that mimics acute myocardial infarction commonly in the absence of obstructive coronary artery disease; it is characterized by temporary left ventricular dysfunction, regularly in a circumferential apical, midventricular, or basal distribution. Considering its acute clinical presentation, coronary angiography with left ventriculography constitutes the gold standard diagnostic tool to exclude or confirm TTS. Frequently, TTS is related to severe emotional or physical stress and a subsequent increased adrenergic stimulation affecting cardiac function. Beyond clinical presentation, epidemiology, and novel diagnostic biomarkers, this review draws attention to potential pathophysiological mechanisms for the observed reversible myocardial dysfunction such as sympathetic overdrive-mediated multi-vessel epicardial spasms, microvascular dysfunction, the direct toxicity of catecholamines, lipotoxicity, and inflammation. Considering the long-term prognosis, further experimental and clinical research is indispensable to elucidate further pathophysiological mechanisms underlying TTS before randomized control trials with evidence-based therapeutic management can be performed.

Keywords: acute heart failure; biomarker; broken heart syndrome; inflammation; lipotoxicity; takotsubo syndrome.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Cardiac ventriculography of different takotsubo syndrome types during diastole and systole. Hypokinetic region in focal type labeled with an arrow.
Figure 2
Figure 2
CMR images (four-chamber view) demonstrating biventricular ballooning in TTS, thus indicating RV involvement.
Figure 3
Figure 3
T2-weighted images (short-axis view) demonstrating normal signal intensity (SI) of the basal myocardium and global edema of the mid and apical myocardium. SI analysis (bottom row) of the T2-weighted images with color-coded display of relative SI normalized to skeletal muscle (blue indicates an SI ratio of myocardium to skeletal muscle of ≥1.9 or higher, thus indicating edema; green/yellow indicates a normal SI ratio of <1.9).
Figure 4
Figure 4
Pathophysiological mechanisms in TTS. CRH: corticotropin-releasing hormone; ACTH: adrenocorticotropic hormone; cAMP: cyclic adenosine monophosphate; SERCA2a: sarco/endoplasmic reticulum Ca2+-ATPase; β1-AR: β1-adrenoceptor; LV: left ventricular; RWMA: regional LV wall motion abnormality.
See this image and copyright information in PMC

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